His family noticed the personality change first. Over several months, a 21-year-old man became irritable, swung between moods, pulled away from people, and watched his academic performance fall apart. The behavior was different enough from his baseline that he was initially steered toward psychiatric care.
Then his hands started shaking, worse during writing and eating, and his speech grew slightly difficult. Liver tests came back abnormal. And when he finally got a brain MRI, the midbrain showed the outline of a panda's face.
The case appears in Radiology Case Reports under the title "Expanding the spectrum of the giant panda sign: a bright-eye variant in Wilson disease." The panda was there, but its eyes were wrong.
The Sign Radiologists Have Looked For Since 1991
The "face of the giant panda" was first described by Hitoshi and colleagues in 1991 and is treated as characteristic of Wilson disease, an inherited disorder in which mutations in the ATP7B gene block the body from clearing copper. Copper builds up in the liver, brain, corneas and elsewhere.
The illusion depends on a specific combination of signals on axial T2-weighted images through the midbrain. High signal in the tegmentum forms the face. The red nuclei keep their normal darker appearance and read as the eyes. The lateral part of the substantia nigra pars reticulata makes the ears. The superior colliculi stay dark and become the chin.
The critical point is that the eyes are supposed to be dark. They look like eyes precisely because the red nuclei are spared while everything around them lights up.
This Panda's Eyes Were Lit Up
In this patient, the red nuclei and substantia nigra showed increased T2 signal instead of preserved signal, producing what has been called the "panda with bright eyes."
That variant is not new to the literature. A Peruvian team described it in Arquivos de Neuro-Psiquiatria under the heading of a rare sign in Wilson disease. In the current case, the authors treat it as a marker of more extensive brainstem involvement.
The rest of the scan was extensive. Symmetrical T2 and FLAIR hyperintensities appeared in the caudate nuclei, putamina, globus pallidi, thalami, posterior limbs of the internal capsules, the pons, and both the superior and middle cerebellar peduncles. There was restricted diffusion in both globus pallidi and both thalami.
Wider imaging surveys back the pattern. A case series in an Egyptian radiology journal cataloged the range of findings in Wilson disease, including the bright claustrum sign and the smaller "miniature panda" in the pons.
MRI abnormalities turn up in nearly all patients with neurological symptoms, and the basal ganglia are the usual first stop. What varies is how far the changes extend and which named pattern, if any, emerges. Signs like the panda are memorable precisely because they are pictorial, but they are shorthand for an underlying distribution of tissue injury, and that distribution does not always arrange itself into a recognizable face.
Low Ceruloplasmin, Copper Rings, and a Diagnostic Score
Imaging alone does not make the diagnosis. His ceruloplasmin, the protein that carries most circulating copper, came back at 8 mg/dL, well below normal. An eye examination found Kayser-Fleischer rings in both eyes, the greenish-brown corneal deposits that form when copper collects at the edge of the cornea.
Those findings, combined with his abnormal liver tests and neurological signs, were scored using the Leipzig criteria, the standard system for phenotypic classification of Wilson disease. The score confirmed the diagnosis.
He was started on D-penicillamine, a chelating drug that binds copper and increases its excretion in urine, along with zinc. His neurological symptoms improved over the following three to four months. The authors describe the recovery at follow-up as partial and say longer-term imaging results are still pending. Written consent for publication of the case and its images was obtained from the patient's parents.
Why the Panda Is Not a Diagnosis by Itself
Timing is the whole story with this disease. Wilson disease is treatable, and chelation started early can halt progression, but the neurological damage that accumulates while a young person is being managed for a presumed psychiatric problem is not always recoverable. As a review in Nature Reviews Disease Primers lays out, presentations range from purely hepatic to purely neurological, and behavioral changes frequently arrive before anything obviously neurological does.
The panda sign is also not exclusive to Wilson disease. A case report in BJR Case Reports documented the same appearance in a patient with a very different clinical picture, and other causes have been described. Bright red nuclei in particular have been reported in metronidazole neurotoxicity, which means the variant seen here is a prompt to look harder rather than a verdict on its own.
This is a single patient, and a case report cannot establish how often the bright-eyed variant occurs or whether it tracks with disease severity, treatment response or duration of illness. What it does is widen the visual vocabulary. A clinician trained to look only for dark panda eyes may not recognize the same disease when the eyes are shining.
Key Questions Answered
What is the face of the giant panda sign?
A pattern on axial T2-weighted MRI of the midbrain in which bright signal in the tegmentum surrounds darker red nuclei and substantia nigra, forming what looks like a panda's face. It is considered characteristic of Wilson disease.
What made this scan different?
The red nuclei and substantia nigra showed increased signal rather than preserved signal, producing the rarer "panda with bright eyes" appearance.
What is Wilson disease?
An inherited disorder caused by ATP7B gene mutations that impair the body's ability to clear copper, allowing it to accumulate in the liver, brain, corneas, and other organs.
Why was he first sent toward psychiatry?
His earliest symptoms were behavioral: irritability, mood swings, social withdrawal, and falling academic performance. Behavioral changes often precede recognizable neurological signs in this disease.
How was the diagnosis confirmed?
Low ceruloplasmin at 8 mg/dL, Kayser-Fleischer rings in both eyes, abnormal liver tests, and neurological findings, scored using the Leipzig criteria.
Is Wilson disease treatable?
Yes. This patient improved over three to four months on D-penicillamine and zinc. Early treatment can halt progression, which is why recognizing the disease before extensive brain involvement matters.
